 Rinderpest (RP) is an acute or subacute,

contagious viral disease of ruminants and swine.

 Disease was instrumental in the establishment
of the first veterinary college in 1762 in Lyon,
France
 Also known as “cattle plague”
 Rinderpest is characterized by high fever,
lachrymal discharge, inflammation, hemorrhage,
necrosis, erosions of the epithelium of the mouth
and of the digestive tract, profuse diarrhea, and
death.
 The “four D’s” of Rinderpest:
 Depression
 Diarrhoea
 Dehydration
 Death
 Rinderpest, the most dreaded
bovine plague known, has changed
the course of history many times over.

Mortality varies from 25%-90%, depending on the strains

of virus and the resistance of the animals.
 Family Paramyxoviridae
 Genus Morbillivirus
 Immunologically related with other members of the
family include
◦ Peste des Petits Ruminants virus (PPR in sheep
and goat)
◦ Measles virus ( in humna)
◦ Canine distemper virus ( In dog)
◦ Phocid distemper virus (sea mammals)
 Relatively fragile virus
• All cloven-hoofed animals are
susceptible (not all are
clinical)
• Most clinical cases occur in
cattle and water buffalo
 Sheep, goats, and yak are mostly subclinical

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Rinderpest
 Most cloven-footed wild animals such as bison
and deer
 Antelope
 Wildebeest
 Giraffe
 Hippopotamus
 Warthog

RINDERPEST HAS NOT BEEN REPORTED SINCE JUNE

1995 IN OUR COUNTRY.

Rinderpest
 Rinderpest virus is quite fragile
The virus is excreted by infected animals in urine,
faeces, nasal discharges, and sweat
 Direct contact
◦ Nasal/ocular secretions
◦ Faeces, urine, saliva, and blood
 Contaminated food or water
 Indirect contact
◦ Fomites
 Most infectious period: 1-2 days before
clinical signs and 8-9 days after onset of
clinical signs
 Varies with strain of RPV, dosage, and route
of exposure (3-15 days)

 Mortality is 100 % in exotic breeds and

20-50 % mortality in indigenous breeds
The virus has a high degree of affinity for
lymphoid tissue and alimentary mucosa.
There is a pronounced destruction of
lymphocytes in tissues.
Inhalation

Disseminate the virus to

other lymphoid organs,
the lungs, and epithelial
cells of mucous
membranes
 PATHOGENESIS
• There is a pronounced destruction of lymphocytes
in tissues. This is the cause of marked
leukopaenia. The virus is intimately associated
with leukocytes, only a small proportion being free
in plasma.
• The focal, necrotic stomatitis and enteritis are
the direct result of the viral infection and
replication in the epithelial cells in the alimentary
tract
 Since the virus induces a strong antibody response
shortly after infection, there is a rapid decrease and
elimination of virus from the body as the clinical signs
and lesions become visible.
 Death is usually from severe dehydration, but in less
acute cases, death may be from activated latent
parasitic or bacterial infections. These aggravate
because the animal is immunosuppressed as a result of
the destruction of lymphoid organs by the virus.
 Fever
 Restlessness, dryness of muzzle
 Photophobia
 Depression
 Nasal & lachrymal secretion
 Congested mucosa
 Mucosal erosions
 Severe diarrhea
 Leucopenia ( TLC < 4000/µl)
 Death
The case definition of rinderpest is ocular and nasal
discharges with any two of the additional signs:

+ fever
+ erosions in the mouth
+ diarrhea
+ dehydration
+ death
Two major forms of disease
◦ Acute or Classic form
◦ Peracute form

Rinderpest
 Most often found in highly
susceptible young and newborn
animals
 High fever (104-107 °F)
 Congested mucous membranes

Rinderpest
 Acute (classic) form characterized
by pyrexia, erosive stomatitis,
gastroenteritis, dehydration, and
death
 Ocular and nasal discharge

Rinderpest
“Shooting” diarrhea

Rinderpest
 Early
serous
ocular
discharge
(Epiphora)

Rinderpest
Depression
Diarrhea
Dehydration
Death

Rinderpest
 Photophobia
 Conjunctivitis

Rinderpest
Immunity after a natural infection is
long and persists for life. The
protection is associated with the
induction of humoral antibodies, first
IgM, and later IgG and IgA.
 Affinity for
• lymphoid tissue
• epithelial tissues of the gastrointestinal tract

 Two system mainly affected are

 Lymphoid tissue (Immune system)
 Digestive system
(Vesicles are not formed in this
disease)
 Necrosis of lymphocytes
 Striking in microscopic sections of lymph nodes,
spleen, and Peyer's patches
 Fragmentation of nuclei of lymphocytes (first
seen) in the germinal centres, and in a short
time, most of the mature lymphocytes disappear
 Multinucleated giant cells containing
eosinophilic cytoplasmic inclusion bodies
 Grossly, changes are most marked in the Peyer's
patches
 Darkened with haemorrhages and slough out,
leaving deep craters (ulcers) in the intestinal
wall.
Hemorrhagic mesenteric lymph nodes

Rinderpest
 Ileum. The mucosa is hemorrhagic and
edematous
Hemorrhagic Peyer’s patches

Rinderpest
epithelial cells in
deep layers of the
stratum malpighii
 The erosions are shallow, with a red raw
floor, and a sharply demarcated margin.
 The lesions in the oral mucosa have a
selective distribution: inside the lower
lip, the adjacent gum, the cheeks near
commissures, and the ventral surface of
the free portion of the tongue.
Early focal mucosal erosions

Rinderpest
Inflammation and necrosis of cheek papillae

Rinderpest
Inflammation of cheek papillae

Rinderpest
Mucosal erosions – “cigarette burns”

Rinderpest
Purulent discharges

Rinderpest
Purulent discharges

Rinderpest
 Excessive Salivation

Rinderpest
Rinderpest: nose with foul
discharge
oral mucosa. There are numerous erosions on
and between the buccal papillae
Rinderpest
Extensive mucosal erosion

Rinderpest
Erosion under the tongue

Rinderpest
Eroded hard palate

Rinderpest
 Oesophagus
◦ Brown and necrotic foci
 Omasum(Rarely erosions and
hemorrhage)
 Abomassum-Most common sites of the
lesions which are most severe in the
pyloric region.
Folds are thick and oedematous and
there may be congestion and Necrosis
 SMALL INTESTINE
 Duodenum and ileum showsstreaks of
haemorrhages and erosions
• PEYER'S PATCHES
Exceptionally vulnerable
 Become so necrotic that patches slough
out, leaving deep raw craters(ulcers) in
the intestinal wall
 LARGE INTESTINE
 Prominent lesions are in the ileo-caecal
valve, caeco-colic junction, and the
rectum
 Linear haemorrhages on the folds of
mucosa of rectum appear like 'Zebra
marking which is pathognomonic in
Rinderpest.
 Ulceration and diphtheitic patches are
also seen.
 Liver: Chronic passive congestion resulting
from cardiac and pulmonary complications
 Subepithelial and subendocardial
haemorrhages
 Purulent conjunctivitis and ulceration of
cornea.
Gastro-enteritis

Rinderpest
Linear petaechial haemorrhages in colon

Rinderpest
Rinderpest: capillary stasis in
rectum (“zebra stripes”)
Multiple longitudinal linear hemorrhages
“Zebra striping” in the colon

Rinderpest
Peyer's patches are depressed and covered by
fibrinonecrotic exudate.
 Colon-The mucosa is edematous and
contains many small hemorrhages and
shallow erosions.
Rinderpest
Trachea-The mucosa is hyperemic and
covered by abundant mucopurulent
exudate.
 Dilatation of capillaries and blood
vessels, congestion and haemorrhages
 Necrosis and infiltration of
inflammatory cells in the affected parts
 Multinucleated giant cells found in the
stratum spinosum (oral mucosa)
 Necrosis, Congestion and
Haemorrhages erosions are found in
the GI tract.
 Clinical, gross, and microscopic
features of the disease are
adequate for a presumptive
diagnosis.
 Immunological methods AGID, ELISA
 Moleculaer techaniques likes PCR
 Isolation and confirmation of virus

Rinderpest
 Bovine virus diarrhea
 Mucosal disease
 Infectious bovine rhinotracheaitis
 Malignant catarrhal fever
 Vesicular stomatitis
 Foot-and-mouth disease
 Salmonellosis
 Necrobacillosis
 paratuberculosis
 Bluetongue / EHD
 Mycotic Stomatitis
Rinderpest